Abstract
Implementation of protocolized surveillance, diagnosis, and management of septic patients, and of surgical sepsis patients in particular, is shown to result in significantly increased numbers of patients surviving their initial hospitalization. Currently, most surgical sepsis patients will rapidly recover from sepsis; however, many patients will not rapidly recover, but instead will go on to develop chronic critical illness (CCI) and experience dismal long-term outcomes. The elderly and comorbid patient is highly susceptible to death or CCI after sepsis. Here, we review aspects of the Persistent Inflammation, Immunosuppression, and Catabolism Syndrome (PICS) endotype to explain the underlying pathobiology of a dysregulated immune system in sepsis survivors who develop CCI; then, we explore targets for immunomodulatory therapy.
Highlights
Sepsis remains one of the leading causes of death in the United States [1]
PMN-Myeloid-derived suppressor cells (MDSCs) are defined as CD11b+ CD14− CD15+ CD66b+ LOX-1+ with low side scatter (SSC), and M-MDSCs are defined as CD14+ CD15− HLA-DR−/lo with low SSC [83]
Though there are no current clinical trials targeting MDSCs in sepsis, future trials should take into account the timing of MDSC modulatory treatment, as the MDSC immunosuppressive function is not seen until day 14 after sepsis [86]
Summary
Implementation of the 2004 and 2011 Surviving Sepsis Campaign guidelines, as well as of the Centers for Medicare & Medicaid Services guidelines for sepsis management [2], and an increase in systemic and protocolized surveillance, diagnosis, and management of sepsis, all together led to a significant decrease in early death and an increase in hospital survival [3,4]. This increased initial survival after sepsis is not yet translated to improved long-term outcomes nor full recovery [5,6].
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